ArticleAntimicrobial agents and chemotherapy2010
In vitro system for modeling influenza A virus resistance under drug pressure.
Article in Antimicrobial agents and chemotherapy, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- A novel hollow-fiber infection model (HFIM) for antiviral PK/PD studies of CMV infection.Antimicrobial agents and chemotherapy · 2026Article
- Adamantane-based inhibitors of the influenza A M2 proton channel: structure-based design, biological evaluation, and synthetic approaches.RSC medicinal chemistry · 2026Review
- Molecular biophysics and inhibition mechanism of influenza virus A M2 viroporin by adamantane-based drugs - Challenges in designing antiviral agents.Journal of structural biology: X · 2025Article
- A five-day treatment course of zanamivir for the flu with a single, self-administered, painless microneedle array patch: Revolutionizing delivery of poorly membrane-permeable therapeutics.International journal of pharmaceutics · 2023Article
- Applications of the hollow-fibre infection model (HFIM) in viral infection studies.The Journal of antimicrobial chemotherapy · 2022Review
- Combining LC-MS/MS and hollow-fiber infection model for real-time quantitation of ampicillin to antimicrobial resistance.Future science OA · 2019Article
- Clinical Regimens of Favipiravir Inhibit Zika Virus Replication in the Hollow-Fiber Infection Model.Antimicrobial agents and chemotherapy · 2018Article
- Article
- Profiling the in vitro drug-resistance mechanism of influenza A viruses towards the AM2-S31N proton channel blockers.Antiviral research · 2018Article
- Oseltamivir-zanamivir combination therapy suppresses drug-resistant H1N1 influenza A viruses in the hollow fiber infection model (HFIM) system.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2018Article
- Sofosbuvir (SOF) Suppresses Ledipasvir (LDV)-resistant Mutants during SOF/LDV Combination Therapy against Genotype 1b Hepatitis C Virus (HCV).Scientific reports · 2017Article
- An M2-V27A channel blocker demonstrates potent in vitro and in vivo antiviral activities against amantadine-sensitive and -resistant influenza A viruses.Antiviral research · 2017Article
- Modelling the emergence of influenza drug resistance: The roles of surface proteins, the immune response and antiviral mechanisms.PloS one · 2017Article
- Pharmacokinetic determinants of virological response to raltegravir in the in vitro pharmacodynamic hollow-fiber infection model system.Antimicrobial agents and chemotherapy · 2015Article
- Flipping in the pore: discovery of dual inhibitors that bind in different orientations to the wild-type versus the amantadine-resistant S31N mutant of the influenza A virus M2 proton channel.Journal of the American Chemical Society · 2014Article
- T-705 (favipiravir) induces lethal mutagenesis in influenza A H1N1 viruses in vitro.Journal of virology · 2013Article
- Pharmacodynamic analysis of a serine protease inhibitor, MK-4519, against hepatitis C virus using a novel in vitro pharmacodynamic system.Antimicrobial agents and chemotherapy · 2012Article
- Molecular dynamics simulation directed rational design of inhibitors targeting drug-resistant mutants of influenza A virus M2.Journal of the American Chemical Society · 2011Article
- Zanamivir, at 600 milligrams twice daily, inhibits oseltamivir-resistant 2009 pandemic H1N1 influenza virus in an in vitro hollow-fiber infection model system.Antimicrobial agents and chemotherapy · 2011Article
- Effect of half-life on the pharmacodynamic index of zanamivir against influenza virus delineated by a mathematical model.Antimicrobial agents and chemotherapy · 2011Article
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Authors and funding
9 authors.
Funding
Abstract
One of the biggest challenges in the effort to treat and contain influenza A virus infections is the emergence of resistance during treatment. It is well documented that resistance to amantadine arises rapidly during the course of treatment due to mutations in the gene coding for the M2 protein. To address this problem, it is critical to develop experimental systems that can accurately model the selection of resistance under drug pressure as seen in humans. We used the hollow-fiber infection model (HFIM) system to examine the effect of amantadine on the replication of influenza virus, A/Albany/1/98 (H3N2), grown in MDCK cells. At 24 and 48 h postinfection, virus replication was inhibited in a dose-dependent fashion. At 72 and 96 h postinfection, virus replication was no longer inhibited, suggesting the emergence of amantadine-resistant virus. Sequencing of the M2 gene revealed that mutations appeared at between 48 and 72 h of drug treatment and that the mutations were identical to those identified in the clinic for amantadine-resistant viruses (e.g., V27A, A30T, and S31N). Interestingly, we found that the type of mutation was strongly affected by the dose of the drug. The data suggest that the HFIM is a good model for influenza virus infection and resistance generation in humans. The HFIM has the advantage of being a highly controlled system where multiplicity parameters can be directly and accurately controlled and measured.
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